Prestin amplifies cardiac motor functions

Cardiac cells generate and amplify force in the context of cardiac load, yet the membranous sheath enclosing the muscle fibers-the sarcolemma-does not experience displacement. That the sarcolemma sustains beat-to-beat pressure changes without experiencing significant distortion is a muscle-contraction paradox. Here, we report that an elastic element-the motor protein prestin (Slc26a5)-serves to amplify actin-myosin force generation in mouse and human cardiac myocytes, accounting partly for the nonlinear capacitance of cardiomyocytes. The functional significance of prestin is underpinned by significant alterations of cardiac contractility in Prestin-knockout mice. Prestin was previously considered exclusive to the inner ear's outer hair cells; however, our results show that prestin serves a broader cellular motor function.

Automated summary

The study found that the elastic element - the motor protein prestin plays a role in amplifying actin-myosin force generation in cardiac myocytes, partly explaining the nonlinear capacitance of cardiomyocytes. In addition, the functional significance of prestin is reflected in significant alterations of cardiac contractility in Prestin-knockout mice.